Evidence map›Paper›PMID 20116417›Full record

ArticleToxicology letters2010

Differential regulation of the dioxin-induced Cyp1a1 and Cyp1b1 genes in mouse hepatoma and fibroblast cell lines.

Sudheer R Beedanagari, Robert T Taylor, Oliver Hankinson

Abstract read
In one paragraph

Article in Toxicology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Multigenerational and Transgenerational Effects of Dioxins.International journal of molecular sciences · 2019
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Potential role of epigenetic mechanisms in the regulation of drug metabolism and transport.Drug metabolism and disposition: the biological fate of chemicals · 2013
    Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Sudheer R BeedanagariMolecular Toxicology Program, Dept of Pathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA.
Robert T Taylor
Oliver Hankinson
University of California, Los Angeles · US

Funding

CARCINOGEN ACTIVATION AND SCREENING IN VARIANT CELLSR01CA028868 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HANKINSON, OLIVER NMN · 1985 to 2010
$3.6M
NCI NIH HHS R01 CA028868NCI NIH HHS R01CA28868
6 · The paper itself

Abstract

The xenobiotic metabolizing enzymes Cyp1a1 and Cyp1b1 can be induced by the environmental contaminant 2,3,7,8-tetrachlorodibenzo-rho-dioxin (dioxin) via the aryl hydrocarbon receptor (AhR). These genes are differentially induced by dioxin in different mouse cell lines. In the mouse hepatoma cell line Hepa1c1c7 (Hepa-1), the Cyp1a1 gene is induced to very high levels by dioxin, but the levels of Cyp1b1 mRNA are extremely low and are not inducible by dioxin. The reverse is the case for the mouse embryonic fibroblast cell line C3H10T1/2, in which Cyp1b1 is induced to very high levels by dioxin, but the levels of Cyp1a1 mRNA are extremely low and not inducible by dioxin. However, dioxin treatment leads to the recruitment of AhR to the enhancer regions of both genes in both cell lines. Somatic cell hybrid clones generated between the two cell lines display high levels of induction of both genes in response to dioxin. Strong reactivation of the Cyp1a1 gene was also observed in C3H10T1/2 cell line after treatment with the DNA methyl transferase inhibitor, 5-aza-2'-deoxycytidine (5-AzadC) and the histone deacetylase inhibitor, trichostatin-A (TSA). However, only modest reactivation of Cyp1b1 was observed in Hepa-1 cells after 5-AzadC or TSA treatment. These data demonstrate that the presence or absence of binding of AhR to regulatory regions is not responsible for determining the differences in levels of induction of the two genes in these cell lines and indicate that DNA methylation plays a major role in silencing of Cyp1a1 gene expression in C3H10T1/2 cells, but appears to play only a minor role in silencing Cyp1b1 gene expression in Hepa-1 cells, which likely occurs principally because Hepa-1 cells lack a factor required for high levels of induction of this gene.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsAryl Hydrocarbon HydroxylasesAzacitidineCarcinoma, HepatocellularCell LineCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1DecitabineDioxinsEnzyme InductionFibroblastsHybrid CellsHydroxamic AcidsLiver NeoplasmsMiceAryl Hydrocarbon HydroxylasesAzacitidineCyp1b1 protein, mouseCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1DecitabineDioxinsHydroxamic AcidsReceptors, Aryl HydrocarbonRNA, Messengertrichostatin A

Identifiers

PMID20116417
PMCPMC2839003
OpenAlexW2034069757

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.